General Anesthesia — MCQs

General Anesthesia Indian Medical PG Practice Questions and MCQs

Question 81: What is the chemical formula for laughing gas?

A. N2O (Correct Answer)
B. Lewisite
C. H2S
D. CO2

Explanation: **Explanation:** **Nitrous Oxide (N₂O)**, commonly known as **laughing gas**, is the correct answer. It is a colorless, odorless, and non-flammable inorganic gas used in anesthesia for its analgesic and sedative properties. It acts primarily by inhibiting NMDA receptors and stimulating opioid neurons in the brain. **Analysis of Options:** * **A. N₂O (Correct):** This is the chemical formula for Nitrous Oxide. It is the only inorganic gas used in modern clinical anesthesia. * **B. Lewisite:** This is an organoarsenic compound used as a chemical weapon (blister agent/vesicant). It is not used in anesthesia. * **C. H₂S (Hydrogen Sulfide):** A highly toxic, flammable gas with a characteristic "rotten egg" smell. It is a potent cellular asphyxiant. * **D. CO₂ (Carbon Dioxide):** While used in medicine (e.g., for insufflation during laparoscopy), it is a byproduct of metabolism and not an anesthetic agent. **High-Yield Clinical Pearls for NEET-PG:** 1. **Blood-Gas Partition Coefficient:** N₂O has a low coefficient (0.47), leading to rapid induction and recovery. 2. **Second Gas Effect:** N₂O accelerates the uptake of a co-administered volatile anesthetic. 3. **Diffusion Hypoxia (Fink Effect):** Occurs at the end of surgery when N₂O rapidly diffuses from blood to alveoli, diluting oxygen. Prevention requires 100% O₂ for 5–10 minutes post-discontinuation. 4. **Contraindications:** Because N₂O is 34 times more soluble than Nitrogen, it expands closed air spaces. It is strictly contraindicated in **pneumothorax, intestinal obstruction, air embolism, and middle ear surgeries.** 5. **Vitamin B12:** Chronic exposure inhibits methionine synthase, leading to megaloblastic anemia and peripheral neuropathy.

Question 82: Which of the following fluorinated anesthetic agents does not produce toxic fluoride ions?

A. Sevoflurane
B. Methoxyflurane
C. Desflurane (Correct Answer)
D. Enflurane

Explanation: **Explanation:** The production of inorganic fluoride ions ($F^-$) during anesthesia is a result of the **metabolic degradation** (biotransformation) of fluorinated volatile anesthetics by hepatic cytochrome P450 enzymes (specifically CYP2E1). High levels of serum fluoride (typically >50 µmol/L) are associated with **nephrotoxicity**, manifesting as vasopressin-resistant polyuric renal failure. **Why Desflurane is the correct answer:** Desflurane is characterized by extreme **metabolic stability**. Due to its structure (fluorine substitution of the chlorine atom found in isoflurane), it undergoes minimal metabolism—only about **0.02%** of the absorbed dose is biotransformed. This level is so negligible that it does not produce detectable or clinically significant levels of toxic fluoride ions, making it safe for patients with renal impairment. **Analysis of Incorrect Options:** * **Methoxyflurane:** It is the most extensively metabolized agent (~50%). It produces very high levels of fluoride ions and is notorious for causing dose-related nephrotoxicity. It is no longer used for maintenance of anesthesia. * **Sevoflurane:** It undergoes significant metabolism (~5–8%), releasing fluoride ions. While serum levels can exceed 50 µmol/L, it rarely causes clinical nephrotoxicity, though its reaction with soda lime to form **Compound A** remains a concern. * **Enflurane:** It is metabolized at a rate of ~2–3%. While less toxic than methoxyflurane, it can still elevate fluoride levels, especially after prolonged exposure. **High-Yield Clinical Pearls for NEET-PG:** * **Metabolic Rate Order:** Methoxyflurane (50%) > Halothane (20%) > Sevoflurane (5-8%) > Enflurane (2%) > Isoflurane (0.2%) > **Desflurane (0.02%)**. * **Compound A:** Associated specifically with **Sevoflurane** in CO2 absorbers. * **Carbon Monoxide:** Desflurane produces the highest amount of CO when used with dry/desiccated soda lime. * **Boiling Point:** Desflurane has the lowest boiling point (23.5°C) and requires a special heated vaporizer (Tec 6).

Question 83: Which intravenous anesthetic agent possesses local anesthetic properties?

A. Ketamine (Correct Answer)
B. Propofol
C. Thiopentone
D. Etomidate

Explanation: **Explanation:** **Ketamine** is a unique phencyclidine derivative that acts primarily as an NMDA receptor antagonist. Beyond its systemic effects, ketamine possesses significant **local anesthetic properties**. It exerts this effect by blocking sodium channels in a manner similar to conventional local anesthetics (like Lidocaine). When applied topically or injected locally, it can produce sensory blockade. Clinically, this property is sometimes utilized in "multimodal analgesia" to reduce postoperative pain. **Analysis of Incorrect Options:** * **Propofol:** An alkylphenol that acts via GABA-A receptors. It is notorious for causing **pain on injection** (due to activation of the kinin system), which is the opposite of a local anesthetic effect. * **Thiopentone:** A short-acting barbiturate. It is actually considered **anti-analgesic** in sub-anesthetic doses, meaning it can lower the pain threshold. Accidental intra-arterial injection causes severe vasospasm and necrosis, not anesthesia. * **Etomidate:** An imidazole derivative used for its cardiovascular stability. It has no analgesic or local anesthetic properties and is associated with myoclonus and adrenocortical suppression. **High-Yield Clinical Pearls for NEET-PG:** * **Dissociative Anesthesia:** Ketamine causes a state where the patient appears awake (eyes open) but is unconscious and amnesic. * **Sympathomimetic:** It is the IV anesthetic of choice for **bronchial asthma** and **hypovolemic shock** because it increases HR, BP, and causes bronchodilation. * **Contraindications:** Avoid in patients with raised Intracranial Pressure (ICP) or Intraocular Pressure (IOP), and those with ischemic heart disease. * **Emergence Delirium:** A common side effect characterized by hallucinations, which can be prevented by pre-treating with Benzodiazepines (e.g., Midazolam).

Question 84: Succinylcholine is a/an

A. Intravenous anesthetic agent
B. Non-depolarizing muscle relaxant
C. Short-acting narcotic
D. None of the above (Correct Answer)

Explanation: **Explanation:** The correct answer is **D. None of the above** because Succinylcholine (Suxamethonium) is a **depolarizing neuromuscular blocking agent**. It is the only drug in this class currently used in clinical practice. **Why the options are incorrect:** * **Option A:** Succinylcholine is not an anesthetic agent; it provides no analgesia or unconsciousness. It is a muscle relaxant used to facilitate endotracheal intubation. * **Option B:** Succinylcholine is a **depolarizing** relaxant. It acts as an agonist at the nicotinic acetylcholine receptors (nAChR) at the neuromuscular junction, causing persistent depolarization (manifested as fasciculations) followed by flaccid paralysis. Non-depolarizing agents (e.g., Vecuronium, Atracurium) act as competitive antagonists. * **Option C:** It is not a narcotic (opioid). It has no effect on pain pathways or opioid receptors. **High-Yield NEET-PG Pearls:** 1. **Mechanism:** It mimics acetylcholine but is not degraded by acetylcholinesterase; it is metabolized by **Pseudocholinesterase** (Butyrylcholinesterase). 2. **Onset and Duration:** It has the fastest onset (30–60 seconds) and shortest duration (5–10 minutes), making it the drug of choice for **Rapid Sequence Induction (RSI)**. 3. **Key Side Effects:** Hyperkalemia (avoid in burns, trauma, or denervation injuries), muscle fasciculations, myalgia, and increased intraocular/intragastric pressure. 4. **Malignant Hyperthermia:** Succinylcholine is a known trigger for Malignant Hyperthermia (treated with Dantrolene). 5. **Phase II Block:** Prolonged exposure or high doses can lead to a Phase II block, where the membrane repolarizes but remains insensitive to acetylcholine, behaving like a non-depolarizing block.

Question 85: Non-depolarizing muscle relaxants are potentiated by all except?

A. Phenytoin (Correct Answer)
B. Aminoglycoside antibiotics
C. Polymyxin
D. Quinidine

Explanation: **Explanation:** The potentiation or antagonism of non-depolarizing muscle relaxants (NDMRs) depends on their interaction with the neuromuscular junction (NMJ) and hepatic enzyme induction. **Why Phenytoin is the correct answer:** Phenytoin is a potent **hepatic enzyme inducer**. Chronic administration of phenytoin (and carbamazepine) leads to an increased rate of metabolism of NDMRs (especially vecuronium and rocuronium). Furthermore, it causes an up-regulation of acetylcholine receptors at the NMJ. Both mechanisms lead to **resistance** to NDMRs, meaning higher doses are required and the duration of action is shortened. Therefore, it does not potentiate but rather **antagonizes** the effect. **Why the other options are incorrect:** * **Aminoglycosides (e.g., Neomycin, Gentamicin):** These potentiate NDMRs by inhibiting the pre-junctional release of Acetylcholine (ACh) and reducing post-junctional sensitivity to ACh. * **Polymyxins:** These exert a potent neuromuscular blocking effect by acting like "membrane stabilizers," significantly prolonging the block. * **Quinidine:** This Class IA antiarrhythmic potentiates NDMRs by depressing muscle fiber excitability and decreasing ACh release. **High-Yield Clinical Pearls for NEET-PG:** * **Antibiotics that potentiate NDMRs:** Aminoglycosides, Tetracyclines, Polymyxin, and Lincomycin. (Note: Penicillins and Cephalosporins do **not** have this effect). * **Electrolytes that potentiate NDMRs:** Hypokalemia, Hypermagnesemia, and Hypocalcemia. * **Other potentiators:** Inhalational anesthetics (Desflurane > Sevoflurane > Isoflurane), Local anesthetics, and Hypothermia. * **Acute vs. Chronic Phenytoin:** While chronic use causes resistance, an *acute* IV dose of phenytoin can occasionally potentiate the block. However, for exam purposes, Phenytoin is the classic example of resistance/antagonism.

Question 86: Which of the following is NOT an intravenous anesthetic agent?

A. Etomidate
B. Thiopentone
C. Ketamine
D. Cyclopropane (Correct Answer)

Explanation: **Explanation:** The correct answer is **Cyclopropane** because it is an **inhalational (volatile) anesthetic gas**, not an intravenous agent. Historically used for its rapid induction and maintenance of blood pressure, it has been largely phased out in modern practice due to its high flammability and explosive potential when mixed with oxygen. **Analysis of Options:** * **Etomidate (Option A):** An intravenous induction agent known for its **cardiovascular stability**. It is the drug of choice for hemodynamically unstable patients or those with coronary artery disease. A key side effect is transient adrenal suppression. * **Thiopentone (Option B):** A classic ultra-short-acting **barbiturate** administered intravenously. It was the gold standard for rapid induction for decades. It is contraindicated in patients with porphyria. * **Ketamine (Option C):** An intravenous agent that produces **dissociative anesthesia**. It is unique because it provides potent analgesia and stimulates the sympathetic nervous system, making it useful in hypovolemic shock and asthma. **NEET-PG High-Yield Pearls:** * **Propofol** is currently the most commonly used IV induction agent ("Milk of Amnesia"). * **Cyclopropane** is known for the "Cyclopropane Shock" (post-operative hypotension) and sensitizing the myocardium to catecholamines, leading to arrhythmias. * **Drug of Choice (DOC) Summary:** * Day-care surgery: Propofol * Shock/Trauma: Ketamine or Etomidate * Head injury (to decrease ICP): Thiopentone or Propofol

Question 87: Which of the following inhalation anesthetics causes rapid induction of anesthesia?

A. Isoflurane
B. Halothane (Correct Answer)
C. Desflurane
D. Sevoflurane

Explanation: **Explanation:** The speed of induction of an inhalational anesthetic is primarily determined by its **Blood-Gas Partition Coefficient (BGPC)**. A lower BGPC indicates lower solubility in the blood, leading to a faster rise in alveolar concentration (Fa/Fi ratio) and quicker equilibration with the brain, resulting in rapid induction. **Why Halothane is the Correct Answer (Contextual):** In the context of this specific question, **Halothane** is traditionally recognized for providing a "smooth and rapid" induction, particularly in pediatric practice, because it is non-pungent and does not cause airway irritation (unlike Isoflurane or Desflurane). While modern agents like Sevoflurane are technically faster due to lower solubility, Halothane remains a classic textbook answer for rapid clinical induction due to its lack of pungency and high potency. **Analysis of Options:** * **Isoflurane (A):** Has a BGPC of 1.4. It is pungent and causes airway irritation (coughing, breath-holding), making it unsuitable for rapid mask induction. * **Desflurane (C):** Has the lowest BGPC (0.42), theoretically making it the fastest. However, it is highly pungent and causes sympathetic stimulation/laryngospasm, preventing its use for rapid induction. * **Sevoflurane (D):** Has a low BGPC (0.65) and is non-pungent. In modern practice, it is the agent of choice for rapid inhalational induction. (Note: If both Halothane and Sevoflurane are present, Sevoflurane is pharmacokinetically faster, but Halothane is often the historical benchmark in older MCQ formats). **NEET-PG High-Yield Pearls:** * **Solubility Rule:** Lower Blood-Gas Partition Coefficient = Faster Induction and Recovery. * **Order of Solubility (BGPC):** Halothane (2.4) > Isoflurane (1.4) > Sevoflurane (0.65) > Nitrous Oxide (0.47) > Desflurane (0.42). * **Second Gas Effect:** Nitrous oxide (N₂O) accelerates the uptake of a companion volatile anesthetic. * **Oil-Gas Coefficient:** Determines the **Potency** (MAC) of the drug (Meyer-Overton Hypothesis).

Question 88: Minimum alveolar concentration (MAC) of an anesthetic agent means it produces lack of reflex response to skin incision in what percentage of subjects?

A. 25%
B. 50% (Correct Answer)
C. 75%
D. 100%

Explanation: **Explanation:** The **Minimum Alveolar Concentration (MAC)** is a fundamental concept in inhalational anesthesia, representing the potency of an anesthetic agent. It is defined as the steady-state alveolar concentration of an anesthetic gas (at 1 atmosphere) that prevents gross purposeful movement in response to a standard surgical stimulus (skin incision) in **50% of subjects**. **Why 50% is Correct:** MAC is essentially the **ED50** (Median Effective Dose) for inhalational agents. It provides a standardized measure to compare the potency of different gases; the lower the MAC value, the more potent the anesthetic (e.g., Halothane has a MAC of 0.75%, while Nitrous Oxide is >100%). **Why Other Options are Incorrect:** * **25% (Option A):** This value does not correspond to any standard clinical definition of anesthetic potency. * **75% (Option C):** While higher concentrations increase the depth of anesthesia, 75% is not the statistical benchmark used for MAC. * **100% (Option D):** To ensure 95-99% of patients do not move, clinicians use **MAC-BAR** (Blunt Autonomic Response) or roughly **1.3 MAC**, which is the surgical dose required for most clinical procedures. **High-Yield Clinical Pearls for NEET-PG:** * **MAC-Awake:** The concentration at which 50% of patients respond to verbal commands (usually ~0.3–0.4 MAC). * **Factors that INCREASE MAC (Require more gas):** Hyperthermia, hypernatremia, chronic alcohol abuse, and increased central neurotransmitters (e.g., cocaine, ephedrine). * **Factors that DECREASE MAC (Require less gas):** Hypothermia, pregnancy, acute alcohol intoxication, old age, and concurrent use of opioids or benzodiazepines. * **Meyer-Overton Hypothesis:** States that MAC is inversely proportional to lipid solubility (Oil:Gas partition coefficient).

Question 89: Which of the following is NOT true regarding neurolept analgesia?

A. Can be used along with O2 and N2O
B. Causes focal dystonia
C. Is exemplified by Fentanyl-droperidol
D. None of the above (Correct Answer)

Explanation: **Explanation:** **Neuroleptanalgesia (NLA)** is a state of profound sedation and analgesia produced by the combination of an opioid analgesic and a neuroleptic (antipsychotic) drug. The classic combination used is **Fentanyl** (opioid) and **Droperidol** (butyrophenone neuroleptic). 1. **Why Option D is correct:** All the statements (A, B, and C) are medically accurate descriptions of neuroleptanalgesia. Since the question asks for the statement that is **NOT** true, "None of the above" is the correct choice. 2. **Analysis of Options:** * **Option A:** NLA can indeed be used with **O₂ and N₂O**. When these inhalation gases are added to the fentanyl-droperidol combination, the state is upgraded to **Neurolept anesthesia**, which provides complete unconsciousness suitable for surgery. * **Option B:** Droperidol is a dopamine (D2) receptor antagonist. Like other antipsychotics, it can cause **extrapyramidal side effects**, most notably **focal dystonia** (e.g., oculogyric crisis or torticollis). * **Option C:** The combination of **Fentanyl and Droperidol** (commercially known as Innovar in a 1:50 ratio) is the prototype example of neuroleptanalgesia. **High-Yield Clinical Pearls for NEET-PG:** * **Innovar Ratio:** Contains 0.05 mg Fentanyl and 2.5 mg Droperidol per mL. * **Patient State:** The patient remains conscious, detached from surroundings, and cooperative but feels no pain (quiescence). * **Contraindication:** Avoid in patients with **Parkinson’s disease** due to the dopamine-blocking effects of droperidol. * **Side Effects:** Droperidol can cause **QT interval prolongation**; therefore, ECG monitoring is recommended.

Question 90: Which of the following is a common side effect of ketamine?

A. Emergence delirium (Correct Answer)
B. Pain on injection
C. Bronchoconstriction
D. Depression of cardiovascular system

Explanation: **Explanation:** **Ketamine** is a unique intravenous anesthetic agent that acts as an NMDA receptor antagonist, producing a state known as **dissociative anesthesia**. **1. Why Emergence Delirium is Correct:** Emergence delirium (or emergence reactions) is the most characteristic side effect of ketamine. As the patient recovers from anesthesia, they may experience vivid dreams, hallucinations, illusions, and confusion. This occurs due to the depression of sensory association areas in the brain while the limbic system remains active. It is more common in adults than children and can be minimized by pre-medication with **benzodiazepines** (e.g., Midazolam). **2. Why the Other Options are Incorrect:** * **B. Pain on injection:** This is a classic side effect of **Propofol** and **Etomidate**, not Ketamine. * **C. Bronchoconstriction:** Ketamine is actually a potent **bronchodilator** due to its sympathomimetic effects. It is the induction agent of choice for patients with status asthmaticus. * **D. Depression of cardiovascular system:** Unlike most anesthetics, Ketamine **stimulates** the cardiovascular system (increasing HR, BP, and CO) via indirect sympathetic stimulation. It is the agent of choice for patients in **hypovolemic shock**. **High-Yield Clinical Pearls for NEET-PG:** * **Mechanism:** NMDA receptor antagonist. * **Analgesia:** Provides profound somatic analgesia. * **Reflexes:** Airway reflexes (cough/gag) are usually preserved. * **Contraindications:** Head injury (increases ICP), Intraocular surgery (increases IOP), and Ischemic Heart Disease (increases myocardial oxygen demand). * **Secretions:** Causes significant **hypersalivation**; often co-administered with Glycopyrrolate.

Practice by Chapter

History of Anesthesia

Practice Questions

Preoperative Evaluation

Practice Questions

Pharmacology of Inhalational Anesthetics

Practice Questions

Pharmacology of Intravenous Anesthetics

Practice Questions

Neuromuscular Blocking Agents

Practice Questions

Airway Management

Practice Questions

Endotracheal Intubation

Practice Questions

Difficult Airway Algorithms

Practice Questions

Intraoperative Monitoring

Practice Questions

Depth of Anesthesia Monitoring

Practice Questions

Emergence from Anesthesia

Practice Questions

Postoperative Care

Practice Questions

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